Tanshinone IIA sodium sulfonate protects against cardiotoxicity induced by doxorubicin in vitro and in vivo

被引:63
作者
Jiang, Baohong [1 ]
Zhang, Lin [1 ]
Wang, Yingchun [1 ]
Li, Ming [1 ]
Wu, Wanying [1 ]
Guan, Shuhong [1 ]
Liu, Xuan [1 ]
Yang, Min [1 ]
Wang, Junchen [2 ]
Guo, De-an [1 ]
机构
[1] Chinese Acad Sci, Shanghai Res Ctr Modernizat Tradit Chinese Med, Shanghai Inst Mat Med, Shanghai Inst Biol Sci, Shanghai 201203, Peoples R China
[2] Tongji Univ, Dept Pathol, Dongfang Hosp, Shanghai 200120, Peoples R China
关键词
Doxorubicin; Tanshinone IIA sodium sulfonate; Cardiomyopathy; RAT CARDIAC-CELLS; SALVIA-MILTIORRHIZA; OXIDATIVE STRESS; MICE; CARDIOMYOPATHY; HYPERTROPHY; SUPPRESSION; APOPTOSIS; DAMAGE; MODEL;
D O I
10.1016/j.fct.2009.03.038
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Although doxorubicin (DXR) is an effective antineoplastic agent; the serious cardiotoxicity mediated by the production of reactive oxygen species has remained a considerable clinical problem. Our hypothesis is that tanshinone HA sodium sulfonate (TSNIIA-SS), which holds significant affects on cardioprotection in clinic, protects against DXR-induced cardiotoxicity. In vitro investigation on H9c2 cell line, as well as in vivo study in animal model of DXR-induced chronic cardiomyopathy were performed. TSNIIA-SS significantly increased cell viability and ameliorated apoptosis of DXR-injured H9c2 cells using CCK-8 assay and Hoechst 33342 stain respectively. Furthermore. the cardio-protective effects of TSNIIA-SS were confirmed with decreasing ST-interval and QRS interval by electrocardiography (ECG); improving appearance of myocardium with haematoxylin and eosin (H&E) stain; increasing myocardial tensile strength using tension to rupture (TTR) assay and decreasing fibrosis through picric-sirius red staining comparing with those receiving DXR alone. These data have provided the considerable evidences that TSNIIA-SS is a protective agent against DXR-induced cardiac injury. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1538 / 1544
页数:7
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